Implementation of Exercise Management Services Among Sports Medicine Physicians in the United States.

OBJECTIVE: Assessment of physical activity and exercise prescription has been widely supported by many organizations, yet provision of such services remains limited in the United States. We sought to uncover why such services have not been widely adopted. DESIGN: The American Medical Society for Sports Medicine organized a task force to canvas physicians and survey the American Medical Society for Sports Medicine membership. SETTING: Peer-to-peer and telecommunication discussions and web-based questionnaires. PARTICIPANTS: Sports medicine physicians in the United States. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Percentage of sports medicine physicians who provide exercise management services and mechanisms of billing for exercise management, identify barriers to such services, and identify industry collaborations for promoting physical activity through physicians. RESULTS: Three of 4 sports medicine physicians spend at least 1 min encouraging exercise with patients, using Evaluation and Management codes to bill or receive credit. Exercise counseling is often bundled within other patient care. Few health plans leverage the patient's relationship with a primary care physician to promote exercise. Most employed sports medicine physicians do not receive incentives to incorporate exercise counseling into practice, and only 1 in 6 have decision-making authority to hire an exercise professional. Major obstacles are the lack of a business model and knowledge about exercise prescription. CONCLUSION: The existing E&M codes adequately characterize the work, but physicians desire greater payment or credit for providing exercise management services. Physicians desire to do more exercise prescription, but health system bureaucracy, inadequate support, and economic disincentives are barriers to the provision of exercise management services.

Single-cell transcriptomics of the immune system in ME/CFS at baseline and following symptom provocation.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a serious and poorly understood disease. To understand immune dysregulation in ME/CFS, we use single-cell RNA sequencing (scRNA-seq) to examine immune cells in patient and control cohorts. Postexertional malaise (PEM), an exacerbation of symptoms following strenuous exercise, is a characteristic symptom of ME/CFS. To detect changes coincident with PEM, we applied scRNA-seq on the same cohorts following exercise. At baseline, ME/CFS patients display classical monocyte dysregulation suggestive of inappropriate differentiation and migration to tissue. We identify both diseased and more normal monocytes within patients, and the fraction of diseased cells correlates with disease severity. Comparing the transcriptome at baseline and postexercise challenge, we discover patterns indicative of improper platelet activation in patients, with minimal changes elsewhere in the immune system. Taken together, these data identify immunological defects present at baseline in patients and an additional layer of dysregulation in platelets.

Recovery from Exercise in Persons with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

Background and Objectives: Post-exertional malaise (PEM) is the hallmark of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), but there has been little effort to quantitate the duration of PEM symptoms following a known exertional stressor. Using a Symptom Severity Scale (SSS) that includes nine common symptoms of ME/CFS, we sought to characterize the duration and severity of PEM symptoms following two cardiopulmonary exercise tests separated by 24 h (2-day CPET). Materials and Methods: Eighty persons with ME/CFS and 64 controls (CTL) underwent a 2-day CPET. ME/CFS subjects met the Canadian Clinical Criteria for diagnosis of ME/CFS; controls were healthy but not participating in regular physical activity. All subjects who met maximal effort criteria on both CPETs were included. SSS scores were obtained at baseline, immediately prior to both CPETs, the day after the second CPET, and every two days after the CPET-1 for 10 days. Results: There was a highly significant difference in judged recovery time (ME/CFS = 12.7 ± 1.2 d; CTL = 2.1 ± 0.2 d, mean ± s.e.m., Chi2 = 90.1, p < 0.0001). The range of ME/CFS patient recovery was 1-64 days, while the range in CTL was 1-10 days; one subject with ME/CFS had not recovered after one year and was not included in the analysis. Less than 10% of subjects with ME/CFS took more than three weeks to recover. There was no difference in recovery time based on the level of pre-test symptoms prior to CPET-1 (F = 1.12, p = 0.33). Mean SSS scores at baseline were significantly higher than at pre-CPET-1 (5.70 ± 0.16 vs. 4.02 ± 0.18, p < 0.0001). Pharmacokinetic models showed an extremely prolonged decay of the PEM response (Chi2 > 22, p < 0.0001) to the 2-day CPET. Conclusions: ME/CFS subjects took an average of about two weeks to recover from a 2-day CPET, whereas sedentary controls needed only two days. These data quantitate the prolonged recovery time in ME/CFS and improve the ability to obtain well-informed consent prior to doing exercise testing in persons with ME/CFS. Quantitative monitoring of PEM symptoms may provide a method to help manage PEM.

Plasma metabolomics reveals disrupted response and recovery following maximal exercise in myalgic encephalomyelitis/chronic fatigue syndrome.

Post-exertional malaise (PEM) is a hallmark symptom of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). We monitored the evolution of 1157 plasma metabolites in 60 ME/CFS (45 female, 15 male) and 45 matched healthy control participants (30 female, 15 male) before and after 2 maximal cardiopulmonary exercise test (CPET) challenges separated by 24 hours, with the intent of provoking PEM in patients. Four time points allowed exploration of the metabolic response to maximal energy-producing capacity and the recovery pattern of participants with ME/CFS compared with the healthy control group. Baseline comparison identified several significantly different metabolites, along with an enriched percentage of yet-to-be identified compounds. Additionally, temporal measures demonstrated an increased metabolic disparity between cohorts, including unknown metabolites. The effects of exertion in the ME/CFS cohort predominantly highlighted lipid-related as well as energy-related pathways and chemical structure clusters, which were disparately affected by the first and second exercise sessions. The 24-hour recovery period was distinct in the ME/CFS cohort, with over a quarter of the identified pathways statistically different from the controls. The pathways that are uniquely different 24 hours after an exercise challenge provide clues to metabolic disruptions that lead to PEM. Numerous altered pathways were observed to depend on glutamate metabolism, a crucial component of the homeostasis of many organs in the body, including the brain.

Beta2- and beta3-adrenergic receptor polymorphisms and exercise hemodynamics in postmenopausal women.

We sought to determine whether common genetic variations at the beta2 (beta2-AR, Gln27Glu) and beta3 (beta3-AR, Trp64Arg) adrenergic receptor gene loci were associated with cardiovascular (CV) hemodynamics during maximal and submaximal exercise. CV hemodynamics were assessed in 62 healthy postmenopausal women (20 sedentary, 22 physically active, and 20 endurance athletes) during treadmill exercise at 40, 60, 80, and 100% maximal O2 uptake using acetylene rebreathing to quantify cardiac output. The beta2-AR genotype and habitual physical activity (PA) levels interacted to significantly associate with arteriovenous O2 difference (a-vDO2) during submaximal exercise (P = 0.05), with the highest submaximal exercise a-vDO2 in sedentary women homozygous for the beta2-AR Gln allele and no genotype-dependent differences in submaximal exercise a-vDO2 in physically active and athletic women. The beta2-AR genotype also was independently associated with a-vDO2 during submaximal (P = 0.004) and approximately 100% maximal O2 uptake exercise (P = 0.006), with a 1.2-2 ml/100 ml greater a-vDO2 in the Gln/Gln than in the Glu/Glu genotype women. The beta3-AR genotype, independently or interacting with habitual PA levels, was not significantly associated with any CV hemodynamic variables during submaximal or maximal exercise. Thus it appears that the beta2-AR genotype, both independently and interacting with habitual PA levels, is significantly associated with a-vDO2 during exercise in postmenopausal women, whereas the beta3-AR genotype does not appear to be associated with any maximal or submaximal exercise CV hemodynamic responses in postmenopausal women.

Effect of creatine supplementation and a lacto-ovo-vegetarian diet on muscle creatine concentration.

The purpose of this investigation was to examine the effects of preceding oral creatine monohydrate with a lacto-ovo-vegetarian diet on muscle creatine concentration. Thirty-two healthy men, who regularly consumed an omnivorous diet, were randomly assigned to consume a weight maintaining, lacto-ovo-vegetarian (LOV; n = 16) or omnivorous (Omni; n = 16) diet for 26 days. In addition to their assigned diet, on day 22 of the study, subjects were assigned in a double-blind manner to receive either creatine monohydrate (CM; 0.3 g kg d 1 + 20 g Polycose) or an equivalent dose of placebo (PL) for 5 days. There were no significant differences between the LOV and Omni groups at baseline with respect to age, height, and weight. The results demonstrated that consuming a LOV diet for 21 days was an effective procedure to decrease muscle creatine concentration (p <.01) in individuals who normally consume meat and fish in their diet. However, muscle total creatine (TCr) following creatine supplementation did not differ statistically between LOV and Omni diet groups (148.6 4.5 vs. 141.7 4.5 mmol kg-1 d.m.).

Angiotensinogen M235T polymorphism associates with exercise hemodynamics in postmenopausal women.

We sought to determine whether the M235T angiotensinogen (AGT) polymorphism, either interacting with habitual physical activity (PA) levels or independently, was associated with cardiovascular (CV) hemodynamics during maximal and submaximal exercise. Sixty-one healthy postmenopausal women (16 sedentary, 21 physically active, and 24 endurance athletes) had heart rate (HR), blood pressure (BP), cardiac output, stroke volume (SV), total peripheral resistance (TPR), and arteriovenous O2 difference (a-vDO2) assessed during 40, 60, 80, and approximately 100% of VO2 max treadmill exercise. VO2 max did not differ among AGT genotype groups; however, maximal HR was 14 beats/min higher in AGT TT than MM genotype women (P < 0.05). AGT TT genotype women also had 19 beats/min higher HR during approximately 100% VO2 max exercise than AGT MM genotype women (P = 0.008). AGT genotype also interacted with habitual PA levels to associate with systolic BP and a-vDO2 during approximately 100% VO2 max exercise (both P < 0.01). AGT TT genotype women had 11 beats/min higher HR during submaximal exercise than MM genotype women (P < 0.05). AGT genotype interacted with habitual PA levels to associate with systolic BP during submaximal exercise (P = 0.009). AGT genotype, independently or interacting with habitual PA levels, did not associate significantly with diastolic BP, cardiac output, SV, or TPR during maximal or submaximal exercise. Thus this common genetic variant in the renin-angiotensin system appears to associate, both interactively with habitual PA levels and independently, with HR, systolic BP, and a-vDO2 responses to maximal and submaximal exercise in postmenopausal women.

ACE insertion/deletion polymorphism and submaximal exercise hemodynamics in postmenopausal women.

We sought to determine whether the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism is associated with submaximal exercise cardiovascular hemodynamics. Postmenopausal healthy women (20 sedentary, 20 physically active, 22 endurance athletes) had cardiac output (acetylene rebreathing) measured during 40, 60, and 80% VO(2 max) exercise. The interaction of ACE genotype and habitual physical activity (PA) level was significantly associated with submaximal exercise systolic blood pressure, with only sedentary women exhibiting differences among genotypes. No significant effects of ACE genotype or its interaction with PA levels was observed for submaximal exercise diastolic blood pressure. ACE genotype was significantly associated with submaximal exercise heart rate (HR) with ACE II having approximately 10 beats/min higher HR than ACE ID/DD genotype women. ACE genotype did not interact significantly with habitual PA level to associate with submaximal exercise HR. ACE genotype was not independently, but was interactively with habitual PA levels, associated with differences in submaximal exercise cardiac output and stroke volume. For cardiac output, ACE II genotype women athletes had ~25% greater cardiac output than ACE DD genotype women athletes, whereas for stroke volume genotype-dependent differences were observed in both the physically active and athletic women. ACE genotype was not significantly associated, either independently or interactively with habitual PA levels, with submaximal exercise total peripheral resistance or arteriovenous O(2) difference. Thus the common ACE locus polymorphic variation is associated with many submaximal exercise cardiovascular hemodynamic responses.